The long-range objective of this proposal is to define the relationships between observed size and location of experimentally produced myocardial infarcts mapped in detail at autopsy in dogs, quantitative regional wall motion seen on biplane ventriculograms, detailed ECG body surface maps, and epicardial and intramyocardial activation maps. Preliminary work in each of these areas by the co-investigators has suggested that a quantitative interrelationship may exist. The first specific hypothesis to be tested by the experiments proposed is: The magnitude, spatial distribution and timing of ECG surface potentials are quantitatively related to the location and extent of the myocardial infarction, i.e., (a) In the presence of a normally functioning Purkinje system and for any local heart region, the volume over time of a difference map generated between control and post infarct observation is a function of infarct size and (b) The location on the body surface of this difference potential is a function of location of the infarct, and (c) The size and location of the "Q area" on these difference maps is a function of size and location of subendocardial involvement. The volume of the late R wave is inversely related to the extent of mural involvement. The second specific hypothesis to be tested is that the extent and magnitude of distortions of regional wall motion on biplane left ventricular angiograms is quantitatively related to the extent of chronic myocardial infarction or scarring in that wall. Total body surface maps and ventriculograms will be done before, one week after and six weeks after acute infarction. These will be correlated with epicardial and intramyocardial ventricular excitation maps and with gross and microscopic pathogical maps of the extent of myocardial infarct in 5 mm heart cross-sections at autopsy.